Abstract

Phagocytosis is one of the earliest cellular functions, developing approximately 2 billion years ago. Although FcR-based phagocytic signaling is well-studied, how it originated from ancient phagocytosis is unknown. Lipid redistribution upregulates a phagocytic program recapitulating FcR-based phagocytosis with complete dependence on Src family kinases, Syk, and phosphoinositide 3-kinases (PI3K). Here we show that in phagocytes, an atypical ITAM sequence in the ancient membrane anchor protein Moesin transduces signal without receptor activation. Plasma membrane deformation created by solid structure binding generates phosphatidylinositol 4,5-bisphosphate (PIP2) accumulation at the contact site, which binds the Moesin FERM domain and relocalizes Syk to the membrane via the ITAM motif. Phylogenic analysis traces this signaling using PI3K and Syk to 0.8 billion years ago, earlier than immune receptor signaling. The proposed general model of solid structure phagocytosis implies a preexisting lipid redistribution-based activation platform collecting intracellular signaling components for the emergence of immune receptors.

Details

Title
A phosphatidylinositol 4,5-bisphosphate redistribution-based sensing mechanism initiates a phagocytosis programing
Author
Mu, Libing 1 ; Tu, Zhongyuan 2 ; Lin, Miao 3 ; Ruan, Hefei 1 ; Kang, Ning 1 ; Hei, Yongzhen 4 ; Chen, Jiahuan 1 ; Wei, Wei 5 ; Gong, Fangling 5 ; Wang, Bingjie 6 ; Du, Yanan 6 ; Ma, Guanghui 5 ; Amerein, Matthias W 7 ; Xia, Tie 1 ; Shi, Yan 8 

 School of Life Sciences, Tsinghua University, Beijing, China; Institute for Immunology and Department of Basic Medical Sciences, Beijing Key Lab for Immunological Research on Chronic Diseases, School of Medicine; Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, China 
 Department of Microbiology, Immunology & Infectious Diseases and Snyder Institute, University of Calgary, Calgary, AB, Canada 
 Institute for Immunology and Department of Basic Medical Sciences, Beijing Key Lab for Immunological Research on Chronic Diseases, School of Medicine; Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, China; School of Life Sciences, Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China 
 Institute for Immunology and Department of Basic Medical Sciences, Beijing Key Lab for Immunological Research on Chronic Diseases, School of Medicine; Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, China 
 State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, China 
 Department of Biomedical Engineering, School of Medicine, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University, Beijing, China 
 Department of Cell Biology and Anatomy, University of Calgary, Calgary, AB, Canada; Snyder Institute of Chronic Diseases, University of Calgary, Calgary, AB, Canada 
 School of Life Sciences, Tsinghua University, Beijing, China; Institute for Immunology and Department of Basic Medical Sciences, Beijing Key Lab for Immunological Research on Chronic Diseases, School of Medicine; Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, China; Department of Microbiology, Immunology & Infectious Diseases and Snyder Institute, University of Calgary, Calgary, AB, Canada 
Pages
1-16
Publication year
2018
Publication date
Oct 2018
Publisher
Nature Publishing Group
e-ISSN
20411723
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2120167775
Copyright
© 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.